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At least 883 records · Page 49Linked to original sources
PubMed1989

Comparative effect of recombinant IL-1, -2, -3, -4, and -6, IFN-gamma, granulocyte-macrophage-colony-stimulating factor, tumor necrosis factor-alpha, and histamine-releasing factors on the secretion of histamine from basophils.

Most cytokines possess multiple biologic activities. This study was undertaken to investigate the effect of rIL-1 beta, -2, -3, -4 and -6, IFN-gamma, TNF-alpha, and granulocyte-macrophage (GM)-CSF on basophils from 16 donors and the amount of histamine released was compared with that by partially purified mononuclear cell-derived histamine-releasing factor (HRF) and anti-IgE. We found that only IL-3 and GM-CSF at relatively high doses (50 to 500 ng/ml) released small amounts of histamine (3 to 14%) from two allergic donors. In contrast, both HRF and anti-IgE released significant amounts of histamine from all donors. Other cytokines did not release any measurable quantity of histamine. Simultaneous addition of several cytokines to the basophils also failed to release histamine. IL-3, GM-CSF, and IL-1 can also release histamine at lower concentrations (less than 5 ng/ml) when incubated with basophils in the presence of D2O. Basophils from 6 out of 13 allergic donors released histamine in response to IL-3, whereas three donors responded to IL-1 beta and two responded to GM-CSF. The results of this study demonstrated that although IL-3 and GM-CSF release small amounts of histamine only from a select group of allergic patients, mononuclear cell-derived HRF is more potent in their action and release histamine from normals as well as allergic patients.

Animals↗
PubMed1989

Recombinant human IL-1 alpha and -1 beta potentiate IgE-mediated histamine release from human basophils.

In this study, we have explored the relationship between interleukins and human basophil activation. Previous studies by ourselves and others have found that recombinant human (rh) IL-3 causes histamine release. The ability to release histamine has also been claimed for IL-1 but we cannot confirm this. In experiments with the basophils of 29 donors (excluding one D2O responder), histamine release with 100 ng/ml rhIL-1 alpha was 1.3 +/- 1% (SEM), whereas with rhIL-1 beta, it was 0.8 +/- 1%. Both IL-1 alpha and -1 beta were also used at concentrations of 0.01 to 1000 ng/ml without causing release. Neither increasing the Ca2+ concentration nor adding D2O or cytochalasin B caused IL-1 alpha and -1 beta to become secretagogues. rhIL-1, however, did augment IgE-dependent histamine release. The enhancement was similar with both rhIL-1 alpha and -1 beta, i.e. they were dose-dependent between 0.1 and 3 ng/ml and reached a plateau from 3 to 100 ng/ml. At submaximal histamine release (less than 10%), there was enhancement of three IgE-dependent secretagogues: 125% with goat anti-human IgE (n = 7), 215% with Ag E (n = 10), and 260% with a histamine releasing factor (n = 7). Non-IgE-dependent stimuli (formyl-methionine-leucine-phenylalanine and the ionophore A23187, n = 10) were enhanced less than 5%. rhIL-1-enhancement persisted after cell washing (n = 10). rhIL-1 was active in preparations of 50 to 75% pure basophils in which mononuclear cells were reduced by greater than 95% (n = 4), and mAbH34 to IL-1 beta blocked the enhancement caused by that molecule. We postulate that basophils have an IL-1 receptor which, when occupied, upregulates the response to IgE-related signals. Thus, this work characterizes a second interaction between interleukins and the cells central to the allergic response.

Adjuvants, Immunologic↗
PubMedDate not supplied

Eosinophil and basophil hypersensitivity to deuterium oxide in atopic asthmatic patients.

Reaction of basophils and eosinophils obtained from venous blood of 35 atopic asthmatics to deuterium oxide was examined "in vitro". Eosinophils were isolated on sodium metrizoate according to Day. Preparation of basophils by centrifuging and washing in Tyrod's solution was performed according to Benveniste. Eosinophils and basophils were degranulated in D2O at the concentration of 44%. Cells were counted in a Fuch-Rosenthal haemacytometer. Basophil degranulation was observed in almost all (25) of patients in which degranulation of eosinophils had been stated. Marked correlation of reaction to D2O between both types of granulocytes was found.

Adult↗
PubMed1989

[Mast cells and basophils in asthma].

Airway inflammation may contribute to the nonspecific bronchial hyperreactivity, which is a prominent feature in chronic asthma. Many stimuli such as allergens in allergic asthma, virus and irritants may induce an early reaction and in some cases a late reaction. An increase of nonspecific bronchial hyperreactivity is well demonstrated after this late reaction but no after the early one. Although a variety of inflammatory cells may be located within the respiratory tract, the late phase is generally considered as a direct consequence of the effects of mediators released from mast cells activated during the early reaction. Eosinophils and other inflammatory cells are attracted by chemotactic mediators such as PGD2. However the pathophysiology of chronic asthma remains uncertain because the heterogeneity of mast cells and the complexity of intercellular regulations. The role of basophils has been suggested mainly because their number increases during the late phase of allergic process. On the other hand, histamine and LTC4, but not PGD2, are found during the late phase: it is well established that basophils do not release PGD2. Two recent hypothesis have focused interest on basophils: the higher releasability property of basophils obtained from allergic and asthmatic patients, whatever their serum IgE and the presence of histamine releasing factors acting only on one kind of IgE (IgE+) which is apparently found in severe asthmatic patients. It may be probable that other cells, such as epithelial cells, play also a prominent role in chronic asthma.

Allergens↗
PubMed1988

Seasonal variation of nasal surface basophilic cells and eosinophils in Japanese cedar pollinosis.

Nasal pollinosis is caused by pollens of trees and grasses as allergen floating in the air during the seasons of blossom. In Japan, cedar pollinosis is the most prevalent of seasonal allergic rhinitis. We studied the seasonal variation of nasal mucosal basophilic cells (cells with basophilic and metachromatic granules) and eosinophils by nasal scraping of cedar pollinosis patients from June 1986 to May 1987, and found that during the season basophilic cells and eosinophils increased significantly, decreased but still remained for two or three monts after the season, and finally disappeared. The variation of eosinophils was more prominent than basophilic cells. The increase of both cells had close correlation with each other.

Adolescent↗
PubMed1987

Bipotential cell differentiation of KU-812: evidence of a hybrid cell line that differentiates into basophils and macrophage-like cells.

KU-812-F is a subclone of KU-812, which has cytological features similar to the parent clone, and which carries the Philadelphia chromosome. We studied the effects of various chemical agents and serum-free culture (SF-C) condition on its differentiation. The KU-812-F subclone differentiated into macrophage-like cells with phorbol myristate acetate (PMA), but not with other agents. Unexpectedly, under SF-C, KU-812-F cells differentiated into mature basophil-like cells, and the histamine content of cell lysates increased in proportion to maturation. The addition of the condensed supernatant of SF-C promoted the cloning efficiency of KU-812-F cells in semisolid SF-C, whereas the cloning efficiency was reduced in SF-C alone. KU-812-F cells expressed myelomonocytic antigens. Additionally, My4 was induced with PMA and SF-C, but less often. HLA-DR was not expressed in any culture conditions, despite blastic morphology of KU-812-F cells or macrophage-like cells induced with PMA. The IgE receptor could not be demonstrated under any conditions. Correspondingly, immature and mature KU-812-F cells did not respond to anti-IgE or concanavalin A (con A), while histamine release was induced with PMA. In conclusion, KU-812-F belongs to the myeloid cell lineage and is at least a bipotential cell that can differentiate into basophils and macrophage-like cells. Although the functions appear to be dissimilar to those of normal basophils, the KU-812-F cell line may be a good model for basophil differentiation. Moreover, KU-812-F cells may provide new insights because they grow in semisolid culture by an autostimulating mechanism.

Basophils↗
PubMed1986

Study of nasal surface basophilic cells in patients with nasal polyp.

Surface basophilic cells in samples obtained from the inferior concha of nasal polyp patients were examined microscopically. Although the cells were believed to be specific to nasal allergy patients, we were also able to observe them in nasal polyp patients without nasal allergy. These cells were found in 5% of normal controls, in 14% of patients with chronic sinusitis without nasal polyp, in 65% with nasal polyp and in 91% with nasal allergy. In patients with unilateral nasal polyp the surface basophilic cells increased on the side with nasal polyp but not on the side without nasal polyp. As the nasal polyp grew in size, so the number of cells grew. After the polyp was removed, the cells decreased appreciably in number. With regard to other nasal diseases, surface basophilic cells were observed in 80% of tracheotomized patients, in 88% of laryngectomized patients due to laryngeal cancer, in 100% of patients with a tumor in nasal cavity, in 100% of patients with irradiation treatment of the nasal cavity and in 90% of patients with atrophic rhinitis. The surface basophilic cells seem to increase in number through some mechanism induced by a blockage of nasal airway by nasal polyp.

Basophils↗
PubMed1987

Sequential development of a conjunctival basophil hypersensitivity lesion in guinea pig.

We investigated the cellular profile of inflammatory infiltrate during development of a guinea pig conjunctival basophil hypersensitivity lesion at 1, 6, 24, 48, and 72 hr following injection of keyhole limpet hemocyanin (KLH). Neutrophils reached maximal accumulation at 6 hr. Eosinophils and basophils reached maximal accumulation at 24 hr. Basophil numbers remained high at 48 hr and were lower at 72 hr. The number of stromal monocytes did not vary significantly from PBS-injected tissues at any time. Mast cell number decreased at 24 hr following antigen challenge. Morphologic evidence for intense secretory activity was seen in cells at the stromal reaction site. Secretion channels and evidence of intense degranulation was seen from electron microscopy of neutrophils, eosinophils, and basophils. Inflammatory cells migrate through the basement membrane into the conjunctival epithelium. After maximal accumulation there was a decrease in the number of inflammatory cell types in the epithelium.

Animals↗
PubMed1985

Vesicular uptake of eosinophil peroxidase by guinea pig basophils and by cloned mouse mast cells and granule-containing lymphoid cells.

Guinea pig basophils, cloned mouse mast cells, and cloned mouse granule-containing lymphoid cells were found to utilize a vesicular transport system to internalize eosinophil peroxidase (EPO) added in vitro. Kinetic analysis indicated that EPO internalization involved the binding of EPO to the plasma membrane, the formation of complex surface invaginations, and the movement of EPO-laden vesicles, tubules, and vacuoles toward the center of the cells. EPO became associated with multivesicular bodies in granule-containing lymphoid cells and mast cells, with immature granules in mast cells, and with mature granules in basophils. In other cells, the endogenous production of granule peroxidases (neutrophils and eosinophils) or the prior uptake of exogenous peroxidatic substances (some basophils) precluded cytochemical analysis of granules for EPO. Vesicular transport of EPO provides a possible explanation for the variable detection of peroxidase activity in mast cells or basophils. It also provides a mechanism for sequestration of this potentially toxic material or for its storage for possible future use.

Animals↗
PubMedDate not supplied

[Correlation of skin test to grass pollen with basophil degranulation test results in 72 patients (author's transl)].

Seventy-two subjects have been tested by skin-test (ST) and human basophil degranulation test (HBDT) with grass pollen extract (GPE). HBDT was done, using a suspension enriched in basophils, by a technic on slide. Results are expressed by an index (DI) which is percentage of basophils having apparently disappeared (i. e. degranulated) in presence of GPE. No less than 100 intact basophils (and often many more) were always counted in absence of GPE (control) for each subject, so that DI higher than 35% are significant (p less than 0,001). DI were higher than 35% in 28 positive ST subjects for at less one of three dilutions of GPE (10(-4), 10(-6), 10(-8)); in the 5 subjects with false-negative result, 3 had a weak ST response. In 39 subjects with negative ST, DI were higher than 35% in two subjects and only for one dilution (10(-4)). So, concordance of results of HBDT and obviously positive ST reaches 94%. In 33 positive ST subjects, a significant correlation appears between DI (at 10(-4) and 10(-6)) and flare diameter and between DI (at 10(-4)) and wheals diameter. HBDT appears to be a suitable and simple technic for routinely study of reaginic allergies.

Basophils↗
PubMed1975

The release of four mediators of immediate hypersensitivity from human leukemic basophils.

The availability of a patient with basophilic leukemia manifesting 75 to 90% mature basophils permitted the use of a cell concentration sufficient to generate and release mediators upon interaction with a calcium ionophore in quantities adequate for their physiocochemical characterization. The mediators were defined in terms of their physicochemical characteristics: slow reacting substance of anaphylaxis (SRS-A) by purification through silicic acid chromatography and inactivation by arylsulfatase; eosinophil chemotactic factor of anaphylaxis (ECF-A) by its gel filtration through Sephadex G-25 and inactivation by subtilisin and not trypsin; and platelet-activating factor (PAF) by its inherent binding to albumin. Both ECF-A and histamine were present in their preformed state, and for histamine it was possible to establish that the concentration per cell was comparable to that of normal human basophils. Dibutyryl cyclic AMP suppressed release of histamine and SRS-A, indicating that their availability was under a control similar to that observed with normal cells subjected to immunologic activation. The demonstration that a suspension of leukemic human basophils contained the preformed mediators, histamine and ECF-A, and generated SRS-A and PAF for release along with histamine and ECF-A, after activation with a calcium ionophore, establishes that a single cell type can serve as a source of the four recognized mediators of immediate-type hypersensitivity.

Aged↗
PubMed1975

Presence of thymic antigen on rabbit basophils.

A goat heteroantiserum specific for a rabbit thymus lymphocyte antigen (RTLA) reacted with rabbit basophils resulting in the release of histamine. This activity was equally absorbed out by thymocytes or basophils. Absorption with either of these cell types also resulted in equal loss of thymocytotoxicity. No effect in either system occurred after absorption with either granulocytes or rabbit fibroblasts. These results could not be explained by the presence of immune complexes or aggregated globulin present in the RTLA antiserum. Further, the RTLA anti-serum had no anti-IgE activity, as demonstrated by its lack of reactivity with mast cells that were otherwise capable of releasing histamine normally after challenge with antigen. We have thus shown a basic difference between mast cells and basophils. We conclude that the rabbit basophil may bear a thymic marker.

Absorption↗
PubMed1979

Dissociation of erythema and basophil accumulation in Jones-Mote type hypersensitivity in the guinea-pig.

Relationship between delayed-in-onset erythema and infiltrating leucocytes in the skin reaction site of Jones-Mote type hypersensitivity was observed in guinea-pigs. Guinea-pigs were immunized with formalin-fixed (F-SRBC) or native form (N-SRBC) of sheep red blood cells in incomplete Freund's adjuvant (IFA). Elicitation was carried out with intradermal injection of F-SRBC or N-SRBC in saline 1 or 3 weeks after immunization. One week after immunization with F-SRBC or N-SRBC in IFA, erythema accompanied by basophil infiltration was detected, but antibody production was negative. Erythema reached a peak at 24 h, but basophil infiltration reached a peak at 48 h or later. In the skin reaction site elicited with N-SRBC, high levels of basophil infiltration were detected persistently even after erythema had disappeared. Three weeks after immunization, low titres of PCA (passive cutaneous anaphylaxis) were detected in guinea-pigs immunized with F-SRBC in IFA. At that time erythematous skin reaction was detected, but the level of basophil infiltration was lower than that of 1 week after immunization. In guinea-pigs immunized with N-SRBC in IFA, skin reaction of the Arthus type accompanied by haemorrhage was observed at the site elicited with N-SRBC.

Animals↗
PubMed1979

The basophil. Its morphology, biochemistry, motility, release reactions, recovery, and role in the inflammatory responses of IgE-mediated and cell-mediated origin.

The current state of our knowledge of basophils is reviewed. Much has recently been learned about these cells-their morphology, biochemical contents, interactions with homocytotropic antibodies, release of mediators in anaphylaxis, capacity for ingesting and releasing exogenous tracers, motility, participation in and progressive degranulation in cell-mediated hypersensitivity reactions, and their recovery from degranulation. It seems unlikely that basophils exist to destroy the organism by anaphylactic shock. Nonetheless, basophil function is probably closely related to the potent chemicals stored in their cytoplasmic granules. Perhaps small amounts of these chemicals are required for homeostasis and these cells function by releasing such substances as they are needed. This hypothesis requires that basophils be capable of releasing their contents slowly and piecemeal, which apparently occurs. This hypothesis also requires that physiological, rather than pharmacological, roles be found for histamine.

Animals↗
PubMed1981

Release of platelet-activating factor (PAF) and histamine. II. The cellular origin of human PAF: monocytes, polymorphonuclear neutrophils and basophils.

The origin of platelet activating factor (PAF) from human leucocytes was investigated. Purified monocytes release PAF passively at pH 10.6, when challenged with Ionophore A 23187 or under phagocytic stimuli. Pure preparations of polymorphonuclear neutrophils liberate PAF passively, when challenged with C5a, neutrophil cationic proteins (CP), their carboxypeptidase B derived products (C5a des Arg, CP des Arg) or under phagocytic stimuli. Basophil rich buffy coat cells release PAF when challenged with C5a, CP, anti-IgE (in low amount) or Synacthen concomitantly with basophil degranulation and histamine release. Electron microscopy studies, carried out on Synacthen-stimulated basophil rich buffy coat, provide morphological evidence for platelet-basophil interaction. In conclusion our data demonstrate that PAF can be released from different leucocyte populations. However, the stimuli able to trigger such release appear to have some specificity for the cell target.

Antigen-Antibody Complex↗
PubMed1981

Anaphylactic degranulation of guinea pig basophilic leukocytes. I. Fusion of granule membranes and cytoplasmic vesicles formation and resolution of degranulation sacs.

Anaphylactic degranulation of guinea pig basophilic leukocytes, induced in vitro either with Concanavalin A or sheep serum (antigen), was resolved by transmission electron microscopy into two phases: (1) fusion of cytoplasmic granule membranes to form degranulation sacs communicating with the extracellular space by narrow pores and (2) resolution of degranulation sacs with concomitant granule matrix extrusion. Fusion of granule membranes occurred in the absence of obvious alterations of cytoplasmic filaments or microtubules but was preceded by a rapid increase in the number of 50- to 70-nm. cytoplasmic vesicles, a process evident 1 minute after exposure to lectin. By 5 minutes and at later intervals up to 20 minutes, as individual granule membranes fused to form degranulation sacs, vesicle frequency plunged to values one-half or less of control levels. Cytoplasmic vesicles were apparently incorporated into degranulation sacs and may have had a role in joining together the membranes of adjacent granules. Histamine release, detected at 5 minutes and maximal at 20 minutes, occurred at times when communications between degranulations sacs and the extracellular space were so narrow as to retain most recognizable granule matrix material. Resolution of degranulation sacs proceeded over a period of a day in culture and, in Concanavalin A-induced anaphylaxis, was sometimes incomplete even after 36 hours. During this phase, the frequency of cytoplasmic vesicles returned to normal or supernormal values, and the thin cytoplasmic processes forming the walls of degranulation sacs developed prominent, longitudinally disposed cytoplasmic filaments and ultimately retracted into the main cell body, depositing the membrane-free cytoplasmic granule matrix material outside the perimeter of the cell. Guinea pig basophil anaphylactic degranulation thus differs morphologically and kinetically from mast cell and basophil degranulation in other species in which granule membrane fusion and granule matrix extrusion occur nearly stimultaneously and are complete within minutes. The guinea pig basophil provides a useful model for dissociating these two intrinsic components of the degranulation process.

Anaphylaxis↗
PubMed1982

Comparison of effects of investigational compounds upon allergic phenomena in rodents in vivo and in human basophils in vitro.

Investigational compounds active in anti-allergic/anti-asthmatic screens in rodents in vivo (IgE-mediated passive cutaneous anaphylaxis in rats, IgE-mediated anaphylactic bronchoconstriction in guinea pigs, and histamine-, or acetylcholine-induced bronchoconstriction in guinea pigs) were examined for their effects against IgE-mediated histamine release from human basophiles. Fifty-seven% (19/33) of investigational compounds active against passive cutaneous anaphylaxis in rats and 40% (12/30) of compounds active against anaphylactic bronchoconstriction in guinea pigs were active also against histamine release from human basophiles. Twenty-eight percent (8/29) and 38% (6/15) of compounds active agonist histamine- and acetylcholine-bronchoconstriction in guinea pigs, respectively, were active also against histamine release from human basophiles. The lack of consistent activity of investigational compounds in the in vivo IgE-mediated anaphylactic screens suggests that diverse inhibitory mechanisms are involved. Anaphylactic histamine release from human basophiles may serve as an adjunct in the determination of the activity profiles of new antiallergic agents. It is of limited value in the search for new bronchodilators.

Acetylcholine↗
PubMed1983

Dissociation of IgE from receptors on human basophils. I. Enhanced passive sensitization for histamine release.

Leukocytes of only one of 11 nonatopic donors could be passively sensitized for histamine release elicited by ragweed extract. A short incubation in an unbuffered isotonic saline at pH 3.9 or in an 0.01 M lactic acid/lactate-buffered isotonic saline at pH 3.9 dissociated from 4 X 10(5) to less than 3 X 10(4) IgE molecules per basophil from washed leukocytes of several in a series of six atopic and 11 nonatopic donors. After such treatment, leukocytes of only one of the 11 nonatopic donors could not be sensitized for histamine release. Basophils of the four ragweed-sensitive donors lost their sensitivity to ragweed after the treatment, but all could be passively resensitized; for three of these donors the level of release approximated their original reactivity. Leukocytes of the two mold-sensitive donors could be passively sensitized to ragweed allergens after but not before treatment. Four plasma samples from histamine release-positive volunteers were used for sensitization of treated leukocytes of each cell donor; three were consistently effective and one was consistently ineffective. The positive plasmas had concentrations of antigen E-specific IgE of over 100 ng/ml, which accounted for 17 to 23% of the total IgE; the inactive one had less than 5 ng/ml of specific IgE. For each cell donor, all three samples of active plasma mediated quite similar histamine release, but there was a spectrum of donor cell reactivity ranging from 23 to 70% release. These results suggest that basophils from each donor, atopic or nonatopic, had a maximal potential for in vitro sensitization, which was only attained if the plasma contained appropriate, but yet to be fully defined, concentrations of specific and total IgE. Several unexpected results were obtained. Treated leukocytes from some individuals were sensitized for mediator release to a greater extent by sixfold diluted than undiluted plasma. In addition, a 4-hr incubation with plasma at 37 degrees C, but not at 25 degrees C or 0 degrees C, was less effective than were shorter incubation periods. Treated leukocytes should be useful in studying kinetic and equilibrium parameters of IgE binding to specific receptors on human basophils. Analogous treatments should also be useful in sensitization and measurement of IgE-receptor interactions of mast cell populations.

Basophils↗